Alternations of the gut microbiota and the Firmicutes/Bacteroidetes ratio after biologic treatment in inflammatory bowel disease.

Biologics Firmicutes/bacteroidetes ratio Gut microbiota Inflammatory bowel disease

Journal

Journal of microbiology, immunology, and infection = Wei mian yu gan ran za zhi
ISSN: 1995-9133
Titre abrégé: J Microbiol Immunol Infect
Pays: England
ID NLM: 100956211

Informations de publication

Date de publication:
01 Oct 2024
Historique:
received: 07 05 2024
revised: 09 09 2024
accepted: 27 09 2024
medline: 12 10 2024
pubmed: 12 10 2024
entrez: 11 10 2024
Statut: aheadofprint

Résumé

The inflammatory bowel disease (IBD), comprising Crohn's disease (CD) and ulcerative colitis (UC) is a complex disease with multifactorial etiology. The intestinal dysbiosis have been investigated to play an important role in IBD pathogenesis and disease activity. The aim of our study was to analyze the intestinal microbiota composition in IBD across different severity levels and the impact of biologic therapy on microbiota modulation. In this study, 27 IBD patients were recruited, including 14 patients undergoing biologic therapy for moderate to severe disease activity and 13 controls with inactive disease. The gut microbial composition was determined by 16 S ribosomal RNA gene sequencing of stool samples. Biologic therapy led to significant clinical improvement in IBD disease activity after 48 weeks. About species richness, community alpha diversity was significant lower in active CD patients and enriched gradually after biologic therapy. The beta-diversity regard to the difference of bacterial community composition showed significant difference between patients in biologic and control group. A decrease in Firmicutes and increase in Bacteroidetes abundance were observed in patients with active disease, both in CD and UC. Biologic treatment induced shifts in gut microbiota, with increased Firmicutes and decreased Bacteroidetes, as well as improved F/B ratio gradually after treatment, correlating with disease activity. Our study suggested that gut microbiota differences changed after biologic therapies among IBD with different disease activity, and a rising Firmicutes/Bacteroidetes ratio could be a potential predictor for disease activity and treatment response monitoring.

Sections du résumé

BACKGROUND BACKGROUND
The inflammatory bowel disease (IBD), comprising Crohn's disease (CD) and ulcerative colitis (UC) is a complex disease with multifactorial etiology. The intestinal dysbiosis have been investigated to play an important role in IBD pathogenesis and disease activity. The aim of our study was to analyze the intestinal microbiota composition in IBD across different severity levels and the impact of biologic therapy on microbiota modulation.
METHODS METHODS
In this study, 27 IBD patients were recruited, including 14 patients undergoing biologic therapy for moderate to severe disease activity and 13 controls with inactive disease. The gut microbial composition was determined by 16 S ribosomal RNA gene sequencing of stool samples.
RESULTS RESULTS
Biologic therapy led to significant clinical improvement in IBD disease activity after 48 weeks. About species richness, community alpha diversity was significant lower in active CD patients and enriched gradually after biologic therapy. The beta-diversity regard to the difference of bacterial community composition showed significant difference between patients in biologic and control group. A decrease in Firmicutes and increase in Bacteroidetes abundance were observed in patients with active disease, both in CD and UC. Biologic treatment induced shifts in gut microbiota, with increased Firmicutes and decreased Bacteroidetes, as well as improved F/B ratio gradually after treatment, correlating with disease activity.
CONCLUSIONS CONCLUSIONS
Our study suggested that gut microbiota differences changed after biologic therapies among IBD with different disease activity, and a rising Firmicutes/Bacteroidetes ratio could be a potential predictor for disease activity and treatment response monitoring.

Identifiants

DOI: 10.1016/j.jmii.2024.09.006 PMID: 39393964
pubmed: 39393964
pii: S1684-1182(24)00184-1
doi: 10.1016/j.jmii.2024.09.006
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024. Published by Elsevier B.V.

Déclaration de conflit d'intérêts

Declaration of competing interest All authors declared there was no conflict of interests.

Auteurs

Yu-Chieh Tsai (YC)

Diversion of Hepatogastroenterology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan. Electronic address: plshfrost@hotmail.com.

Wei-Chen Tai (WC)

Diversion of Hepatogastroenterology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan; Chang Gung University College of Medicine, Taoyuan City, Taiwan. Electronic address: luketai1019@gmail.com.

Chih-Ming Liang (CM)

Diversion of Hepatogastroenterology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan; Chang Gung University College of Medicine, Taoyuan City, Taiwan. Electronic address: gimy54861439@gmail.com.

Cheng-Kun Wu (CK)

Diversion of Hepatogastroenterology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan; Chang Gung University College of Medicine, Taoyuan City, Taiwan. Electronic address: eggclimb@cgmh.org.tw.

Ming-Chao Tsai (MC)

Diversion of Hepatogastroenterology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan; Chang Gung University College of Medicine, Taoyuan City, Taiwan. Electronic address: tony0779@gmail.com.

Wan-Hsiang Hu (WH)

Division of Colorectal Surgery, Department of Surgery, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan; Chang Gung University College of Medicine, Taoyuan City, Taiwan. Electronic address: gary1@cgmh.org.tw.

Pao-Yuan Huang (PY)

Diversion of Hepatogastroenterology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan. Electronic address: paoyuan813@gmail.com.

Chien-Hung Chen (CH)

Diversion of Hepatogastroenterology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan; Chang Gung University College of Medicine, Taoyuan City, Taiwan. Electronic address: e580306@ms31.hinet.net.

Yuan-Hung Kuo (YH)

Diversion of Hepatogastroenterology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan; Chang Gung University College of Medicine, Taoyuan City, Taiwan. Electronic address: 0104kuo@cgmh.org.tw.

Chih-Chien Yao (CC)

Diversion of Hepatogastroenterology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan; Chang Gung University College of Medicine, Taoyuan City, Taiwan. Electronic address: chihchienyao@gmail.com.

Seng-Kee Chuah (SK)

Diversion of Hepatogastroenterology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan; Chang Gung University College of Medicine, Taoyuan City, Taiwan. Electronic address: sengkeechuah@yahoo.com.tw.

Classifications MeSH